Cardiovascular Emergencies - Part 8 pdf

Following a burst of pacing at 180 bpm via a temporar y right ventricular pacing catheter, sinus rhythm is restored with dramatic improvement in ar terial blood pressure bottom tracing..

It is likely that lidocaine will continue to be used as first-linetreatment, particularly for patients exhibiting signs of mildhaemodynamic embarrassment in whom early DCcardioversion would otherwise be considered However, forpatients with reasonably well tolerated VT, there is a strongcase for using either procainamide or sotalol rather thanlidocaine initially (Table 11.4) In general, we would advocate

DC cardioversion if the first antiarrhythmic agent fails toterminate VT There may be occasional exceptions, such aspatients with well tolerated VT who have not responded tolidocaine but in whom immediate DC cardioversion undergeneral anaesthesia may be undesirable because of an ongoingrespiratory tract infection or recent consumption of a meal.Table 11.4 Doses for drug treatment of ventricular

tachycardia

Lidocaine (lignocaine) 1.5 mg/kg over 2 minutes

Procainamide 10 mg/kg at 100 mg/minute

Amiodarone 300 mg (5 mg/kg) over 30 minutes*;

subsequent infusion of 600–1200 mg

over 24 hours

*Into central vein.

In passing, it should be noted that intravenous amiodarone isgenerally unsuitable for termination of VT because of itsrelatively slow onset of action and negative inotropic effectsresulting in a high incidence of haemodynamicdepression/hypotension.21 The major role of amiodarone issuppression of recurrent episodes of VT21, 22(see below)

11.5.3 Antitachycardia pacing

Antitachycardia pacing (ATP) is seldom used as the initialtreatment for VT unless the patient happens to have a

temporary ventricular pacemaker in situ (e.g post-cardiac

surgery) However, it has an invaluable role in the smallminority of patients who present with frequent recurrences of

VT as a simple, painless alternative to multiple cardioversions

Cardiovascular Emergencies

to terminate the attacks while antiarrhythmic drug therapysuch as amiodarone is being introduced to suppress them ATP

is a simple, elegant technique requiring only insertion of astandard temporary transvenous pacing catheter (see Chapter14) plus an external temporary pacemaker with a “3 rate-function” key to deliver pacing at faster rates (typically150–220 bpm) available on most coronary care units.23,24

In the vast majority of cases, sustained monomorphic VT ismediated by re-entrant excitation of a “functional” circuitinvolving a zone of slow myocardial conduction (usuallywithin the border of a healed infarct) The prerequisite forperpetuation of tachycardia in such re-entrant circuits is thepresence of an “excitable gap” of tissue behind the receding

“tail” of electrical activation which has gone through its phase

of refractoriness and recovered excitability in time to bereactivated by the advancing “head”, thereby allowing thenext cycle of the circuit to go ahead Thus, the rationale ofantitachycardia pacing (ATP) is to use an external, temporarypacemaker to stimulate and depolarise the excitable gapcausing the VT to terminate because the advancing head of there-entrant activation encounters refractory tissue Althoughmore complex algorithms are often employed duringintracardiac electrophysiology studies, in the emergencysetting simple overdrive pacing is the easiest method,particularly for non-cardiologists This involves introducing atemporary transvenous pacing catheter and then using anexternal box with the “3” key switched on to deliver a burst

of pacing at 15–20 bpm faster than the VT rate and at arelatively high output (e.g 5.0 V) to ensure capture Typically,the burst is continued for 5–10 seconds with continuous ECGmonitoring until the QRS complexes change morphology(indicating ventricular capture) and the pacing is switched off(Figure 11.14) This technique will terminate 80–90% of cases

of VT slower than 200 bpm However, a minority will accelerate

or degenerate to polymorphic VT or VF and so ATP should only

be delivered with an external defibrillator to hand Ideally, thepatient should also be sedated (e.g with iv midazolam2.5–5 mg) for the first attempt The success of ATP is lower if the

VT rate is above 200 bpm and conversely the chances ofacceleration/degeneration are increased

Unfortunately, generalists are becoming gradually more skilled in temporary cardiac pacing because the number ofcases has steadily declined since the advent of thrombolyticsand the availability of transcutaneous pacing There is anunderstandable reluctance to undertake insertion of atemporary pacemaker and ATP in a patient with recurrent VT,but in reality this is no more challenging than pacing forbradycardia.

de-11.6 Management (step 4): subsequent

management of VT

A detailed account of the investigation and treatment ofpatients with VT is beyond the scope of this book but we willbriefly consider some aspects of management in the acutephase They should all be admitted initially to the coronarycare unit (CCU) for continuous monitoring, and shouldundergo daily 12-lead ECG recordings, measurement of renal

Cardiovascular Emergencies

Figure 11.14 Antitachycardia pacing in VT Recording of sustained monomorphic ventricular tachycardia at 160 bpm Following a burst of pacing at 180 bpm via a temporar y right ventricular pacing catheter, sinus rhythm is restored with dramatic improvement in ar terial blood pressure (bottom tracing).

function electrolytes (particularly serum K and Mg2), and acardiac enzyme series Full cardiac evaluation includingechocardiography (to assess LV function), coronaryangiography, and possibly electrophysiological testing will berequired in most cases and so the admitting medical teamshould liaise with their local cardiologist as soon as possible.The following general comments can be made.

• If there is clear evidence of an ongoing acute coronarysyndrome, this should be treated along conventional lines.However, it should be noted that sustained monomorphic

VT almost invariably arises from the scar of a healed infarct(i.e a fixed electrical substrate) and is rarely triggered byacute myocardial ischaemia (which characteristicallyproduces polymorphic VT or VF) Thus, monomorphic VT

is usually a recurrent problem It is very common to seemodest rises in cardiac enzymes among patients admittedwith monomorphic VT episodes but unless there is clinicaland ECG evidence of an acute MI, this should never bedismissed as a “primary” or early ventricular arrhythmiasecondary to a small infarct which is unlikely to recur (acommon misconception) Most of these patients requireantiarrhythmic drugs or non-pharmacological therapies(implantable cardioverter defibrillators) to protect themagainst recurrent arrhythmias

• Serum Kshould be maintained at > 4.0 mmol/l

• Any proarrhythmic drugs should be withdrawn if possible

• Haemodynamic function should be optimised as thiscontributes to arrhythmogenesis Most patients with VThave impaired LV function and should be on an ACEinhibitor

• If the patient presents with an isolated episode of VT which

is successfully terminated, there is no automaticrequirement to start maintenance antiarrhythmic drugtherapy forthwith and this is often better delayed until thecase can be discussed with a cardiologist (for example, thedrugs may interfere with electrophysiological testing).However, if the patient experiences recurrent attacks of VT,treatment should be started without delay In patients withunderlying coronary artery disease (the majority) the drug

of choice will usually be amiodarone (loading regimen1.2 g/day for 7–10 days) Adjunctive treatment with low-

dose -blockers has been shown to be highly effective inrefractory cases and probably should be consideredroutinely, particularly for patients with LV dysfunction inwhom there is increasing evidence of long-term prognosticbenefit.

• If the attacks are occurring frequently or incessantly,amiodarone can be administered by infusion via a centralvenous catheter for more rapid action although this cancause haemodynamic depression with hypotension orworsening heart failure Even if given parenterally,amiodarone can take up to 72 hours or longer in somecases to achieve therapeutic effect,21,22and it is important towarn the patient, family and nursing staff of the likelyoccurrence of frequent VT episodes during the interveningperiod which will have to be terminated as previouslydiscussed (clearly antitachycardia pacing may beparticularly helpful in this situation if effective).Occasionally, a piggyback infusion of lidocaine (lignocaine)may allow temporary suppression of the VT while thepatient is loaded with amiodarone

11.7 Polymorphic VT, torsade de pointes and the long QT syndromes

Polymorphic VT is a rapid ventricular tachyarrhythmia withconstantly changing morphology of the QRS complexes (incontrast to monomorphic VT) The term torsade de pointesapplies to polymorphic VT arising in the setting of acongenital or acquired long QT syndrome (LQTS) These aremalignant arrhythmias, typically presenting with recurrentsyncope and often degenerating to ventricular fibrillation.Although the ECG appearances of polymorphic VT are quitedistinct from “broad complex tachycardia”, this group ofconditions is considered in this chapter for convenience.25,26

11.7.1 Polymorphic VT without QT prolongation

Polymorphic VT not associated with a long QT syndrome is

most commonly due to myocardial ischaemia in the setting of

Cardiovascular Emergencies

an acute ischaemia (unstable angina, widespread STdepression, etc.), making diagnosis straightforward, but in afew cases recurrent polymorphic VT or VF may developwithout symptomatic angina or striking ECG changes Othercauses of polymorphic VT without LQTS include acutemyocarditis, cardiomyopathies (particularly arrhythmogenicright ventricular dysplasia/cardiomyopathy) and hereditaryion channel disorders such as Brugada syndrome (VT or VFwith RBBB and precordial ST elevation) In contrast to torsade

de pointes (see below), this arrhythmia is triggered by coupled ectopic beats without antecedent cycle lengthchanges Management involves urgent evaluation byechocardiography and coronary angiography and, ifappropriate, anti-ischaemic therapy including -blockers andrevascularisation (emergency PTCA or CABG) For patients inwhom an acute coronary syndrome has been excluded,standard antiarrhythmic agents should be used to control thepolymorphic VT, including lidocaine (lignocaine),amiodarone and -blockers Some of these cases willeventually require implantable defibrillators (ICDs) to protectthem against the risk of sudden death

short-11.7.2 Long QT syndromes and torsade de pointesThese abnormalities of cardiac repolarisation havetraditionally been classified into congenital and acquiredforms of long QT syndrome (LQTS) Congenital LQTS includesthe Romano–Ward syndrome (autosomal dominant) andJervell–Lange–Nielsen syndrome (autosomal recessive withdeafness) and comprise a heterogeneous group of inheritedion channel disorders which predispose the ventricularmyocardium to catecholamine-induced arrhythmias.Typically patients present in childhood or adolescence withsyncope or cardiac arrest triggered adrenergically (suddenfrights, exercise, etc.) and the first-line treatment is -blockers.Acquired LQTS is most commonly due to drug-inducedrepolarisation abnormalities (Box 11.1), but may beexacerbated by bradycardia and/or hypokalaemia In somecases a severe bradyarrhythmia, particularly complete heartblock, or acute myocardial ischaemia is the sole or dominant

causative mechanism In contrast to other forms ofpolymorphic VT, torsade de pointes is characteristicallytriggered by a “short–long–short” sequence consisting of anectopic beat followed by a compensatory pause and thenanother premature beat initiating the tachyarrhythmia (Figure11.15), so called “pause-dependent” or “bradycardia-dependent” initiation Treatment naturally involveswithdrawal of the causative drug plus specific measures tosuppress the tendency to torsade de pointes until ventricularrepolarisation has normalised:

• Increase the heart rate by temporary cardiac pacing (VVI or

AV sequential) or atropine/isoprenaline infusion Thisprevents pause-dependent initiation Usually pacing at orabove 90 bpm will suffice

• Potassium supplementation to maintain serum

K > 4.0 mmol/l Hypokalaemia dramatically exacerbates thepropensity to torsade de pointes

• Magnesium salts at pharmacological doses (e.g magnesiumsulphate 8 mmol bolus followed by 3 mmol/hr) are oftenhighly effective at suppressing drug-related torsade depointes, even in patients without hypomagnesaemia Theexact mechanism has not been elucidated with certainty.Although congenital and acquired LQTS has been equatedrespectively with “adrenergic-dependent” and “pause-dependent” torsade de pointes, these mechanisms are notmutually exclusive Many documented episodes ofpolymorphic VT in congenital LQTS are pause-dependent andmay only respond to combined treatment with pacing and -blockers It is possible that patients who develop acquiredLQTS may have subtle underlying abnormalities of ventricularrepolarisation (forme fruste of congenital LQTS) whichpredispose them to this proarrhythmia

Box 11.1 Causes of long QT syndrome and torsade de

pointes

QT prolonging drugs

• Antiarrhythmic agents (quinidine, disopyramide, sotalol etc.)

• Antimicrobials (macrolide antibiotics, ketoconazole etc.)

• Antihistamines (astemizole, ter fenadine)

• Psychotropic drugs (phenothiazines, haloperidol, tricyclic antidepressants)

Cardiovascular Emergencies

• Cholinergic agonists (cisapride, organophosphates) Bradyarrhythmias

Electrolyte disorders

• Hypokalaemia

• Magnesium depletion Congenital long QT syndromes

Acute myocardial ischaemia

11.7.3 Clinical approach

Both acute and long-term management of polymorphic

VT require specialist input and such cases should be discussedwith the local cardiologist at the earliest possible opportunity.Patients with polymorphic VT and an obvious acute coronarysyndrome should be managed along conventional lines (see Chapter 4) and considered for early coronary angiography/PTCA Cases of acquired LQTS should be managed bywithdrawal of the offending drug/drugs (if any) plus pacing orother measures to accelerate the heart rate, correction ofhypokalaemia and possible magnesium salts Patients thought

to have congenital LQTS with adrenergic triggering should be

Figure 11.15 Long QT syndrome with torsade de pointes Torsade de pointes following a “short–long–short” initiation sequence in a 67 year old woman with chronic renal impairment 24 hours after elective hip

replacement She was taking long-term sotalol 80 mg bd for paroxymal atrial fibrillation and had just completed a 7-day course of clarithromycin for a suspected chest infection The ECG strip shows bradycardia and gross QT prolongation (> 600 ms) with a succession of triggered

ventricular ectopic beats followed by compensatory pauses culminating in

a short run of polymorphic VT She degenerated to VF on two occasions but her arrhythmias were then completely suppressed by atrial pacing at

90 bpm and correction of hypokalaemia (initial serum K 2.9) Pacing was maintained for 48 hours while sotalol and clarithromycin were withdrawn.

immediately commenced on a -blocker (full 24-hour coverage

is required, therefore only long-acting agents such as bisoprolol

or nadolol can be used once daily in this condition, whereasatenolol should be prescribed bd), and catecholamines(isoprenaline, adrenaline (epinephrine), etc.) should be strictlyavoided Patients with polymorphic VT but no evidence ofLQTS or acute ischaemia require urgent evaluation by aspecialist, usually including echocardiography andangiography to check for a “silent” acute coronary syndrome

Clinical cases

Case 11.1

A 74-year-old lady presented complaining of rapid palpitation Her past medical histor y included an anterior myocardial infarction 7 years previously, PTCA/stenting to the right coronar y ar ter y 6 months before admission for chronic stable angina and a diagnosis of ‘paroxysmal SVT’ for 5 years, currently treated with -blockers These infrequent attacks of tachycardia had usually been self-limiting in the past The admission ECG showed a regular, broad complex tachycardia at

180 bpm (Figure 11.1) She was fully conscious and haemodynamically stable, BP 110/60 with no signs of acute hear t failure The presumptive diagnosis was another attack of SVT even though the arrhythmia was not altered by IV adenosine 12 mg However, review of the histor y and ECG on the ward round led to the correct diagnosis of VT It was noted that the ECG showed ver y broad QRS complexes (200 ms), negative concordance and independent P waves with fusion beats (best seen in the V1 rhythm strip) She then under went DC cardioversion and was commenced on amiodarone Retrospective analysis of the ECG tracings of ‘SVT’ in the past showed that these had also been incorrectly classified episodes of VT.

Broad complex tachycardia occurring in the settlng of a prior myocardial infarction is always highly suggestive of VT It is not uncommon for patients with recurrent VT to have picked up an erroneous diagnosis of ‘SVT’ in the past as happened here The fact that the arrhythmia was well tolerated is not helpful in differentiating between VT and SVT In this case, the ECG appearances were also highly suggestive of VT and adenosine testing was not strictly necessar y, but there is no reason why an inexperienced clinician who

is less cer tain about the ECG interpretation, should not resor t to adenosine provocation before reaching a diagnosis – however, doses

of adenosine up to 18–24 mg should have been used and the absence of effect should have led to the default diagnosis of VT.

Cardiovascular Emergencies

Case 11.2

A 65-year-old man with multiple risk factors but no prior histor y of hear t disease presented via his GP with an 8 hour histor y of palpitation and worsening dyspnoea On arrival, he was tachypnoeic

at rest with BP 130/85 but clinical and radiological signs of mild pulmonar y congestion (O2saturation 90% on air) The ECG showed a regular broad complex tachycardia at 200 bpm (Figure 11.16) The admitting SHO was unsure whether the ECG showed evidence of VA dissociation and resor ted to adenosine provocation Bolus doses of

IV adenosine up to 18 mg (maximum tolerated by the patient) failed

to alter the tachycardia and so the default diagnosis of VT was made.

IV lignocaine promptly restored sinus rhythm obviating the need for urgent DC cardioversion Subsequent angiography and electrophysiology studies showed impaired LV function with a chronically occluded LAD and easily inducible VT.

In this case there was no prior histor y of ischaemic hear t disease (although the patient had suffered a silent infarct in the past) but never theless the default diagnosis was VT throughout A more experienced clinician may have concluded that the ECG did show VA dissociation (best seen in the fifth complex which represents a fusion beat), and that the QRS morphology was atypical for classical RBBB with marked left axis deviation, and hence been able to make a confident classification of VT without resor ting to adenosine provocation With respect to management, immediate DC cardioversion would have been the alternative strategy given that the arrhythmia was relatively poorly tolerated, but IV lignocaine had the advantage of speed and simplicity and would not have precluded cardioversion if it had proved ineffective.

Figure 11.16 Sustained monomorphic ventricular tachycardia (see case histor y 11.2).

Case 11.3

A previously fit 26-year-old labourer presented to A & E with abrupt onset of a rapid hear t beat accompanied by central chest tightness and tingling in his left arm Although his blood pressure was 85/55 mmHg, he was warm, well per fused and fully aler t The admission ECG showed a regular broad complex tachycardia of classical LBBB morphology at 220 bpm As the diagnosis was unclear, adenosine was administered at 3, 6 and 12 mg doses but without any effect on the tachycardia Following discussion with the on-call cardiology registrar, a fur ther bolus of IV adenosine 18 mg was administered and terminated the broad complex tachycardia The resting ECG in sinus rhythm showed the characteristic delta wave of Wolff–Parkinson–White syndrome, and the patient was referred for fur ther electrophysiological studies and catheter ablation.

Broad complex tachycardia of classical LBBB morphology in a young, fit patient without prior cardiac disease could well be due to SVT with aberrant conduction and this is the ideal case for adenosine provocation However, it is not uncommon to have to use doses in excess of 12 mg SVT should not be considered “excluded” unless a high dose (if tolerated 24 mg) has failed to slow or terminate the tachycardia.

Case 11.4

A 68-year-old man who had undergone CABG ten years previously was admitted after he had collapsed at home His ECG showed regular broad complex tachycardia at 210 bpm with negative concordance in the chest leads Examination revealed an obese man (> 100 kg) who appeared extremely sick Automated sphygmomanometr y measured his blood pressure at 70/50 and he was shut down and cerebrally obtunded However, he could just open his eyes to command The carotid and femoral pulses were palpable and transcutaneous O2saturation was 98% breathing oxygen at 8 l/min Although there was

no anaesthetist immediately available, it was decided to proceed directly to DC cardioversion in view of his extreme condition He was sedated with IV midazolam 5 mg and fentanyl 25 micrograms and conver ted back to sinus rhythm with a single, synchronised 360 J shock This resulted in prompt and dramatic improvement in his haemodynamic state, with the blood pressure increasing to 140/80 The sedation was reversed with flumazenil 200 micrograms Although the patient grimaced at the time of cardioversion, he had no recollection of the event or receiving a painful shock He was referred for fur ther investigation and subsequently received an implantable cardiover ter defibrillator (ICD).

In an ideal world, DC cardioversion would always be per formed in conjunction with an anaesthetist However, immediate DC cardioversion under neuroleptic sedation may be appropriate for ver y sick patients if no anaesthetist is available Access to

Cardiovascular Emergencies

transcutaneous oxygen saturation monitoring, simple air way management techniques and reversal agents has facilitated this approach The amnesic proper ties of midazolam often result in the patient having no recollection of the event even if they appeared to experience some discomfor t at the time It is preferable to restore sinus rhythm with a single shock if possible and therefore higher delivered energies (200 or 360 J) should be used.

Case 11.5

A 62-year-old man was admitted with a 2 week histor y of recurrent presyncopal episodes, one of which had almost caused him to crash his car He had suffered an uncomplicated inferior MI some 6 months previously He arrived at the A&E depar tment in sinus rhythm but soon after wards went into a broad complex tachycardia at 190 bpm accompanied by profuse sweating and hypotension (75/30 mmHg) The presumptive diagnosis was VT and sinus rhythm was restored by

DC cardioversion under IV propofol and he was commenced on amiodarone 400 mg tds PO However, continuous ECG monitoring showed nonsustained bursts of VT which did not respond to IV lignocaine Two hours later, he went into sustained VT again with hypotension and DC cardioversion was repeated A temporar y pacing catheter was inser ted into the right ventricle for antitachycardia and the amiodarone was switched to an IV infusion via a central venous catheter The patient experienced 16 fur ther symptomatic episodes

of VT over the next 72 hours, all of which were successfully terminated by overdrive pacing The frequency of attacks steadily decreased and once he had been free of VT for 48 hours the pacing catheter was removed Angiography and eletrophysiological studies were per formed once the arrhythmia had been adequately controlled pharmacologically.

Antitachycardia pacing should be considered in any patient with frequent attacks of sustained VT, par ticularly if DC cardioversion has already been used on one or more occasions The purpose of the technique is to terminate episodes of VT and so it must be complemented by pharmacological therapy to suppress the tendency

to ventricular tachycardia.

Summary

In patients with broad-complex tachycardia, par ticularly in those with pre-existing ischaemic hear t disease, VT is the most likely diagnosis Differentiation of VT from SVT should be straightfor ward if simple clinical and ECG guidelines are followed, aided by adenosine testing SVT should only be diagnosed if confirmed by adenosine provocation, i.e termination of arrhythmia or transient slowing of the ventricular rate.

When differentiation of VT from SVT with aberrant conduction is not possible, the default diagnosis should always be VT.

The treatment aim in patients with broad complex tachycardia should

be the restoration of sinus rhythm as soon as possible.

Lidocaine (lignocaine) is the first-line drug of choice owing to safety rather than cardioversion efficacy; second-line agents suitable for use include sotalol and procainamide.

If drug therapy fails to restore sinus rhythm or the patient is haemodynamically compromised, DC cardioversion should be under taken immediately.

Most cases of broad-complex tachycardia/VT should be referred to a cardiologist.

References

1 Stewart RB, Bardy GH, Greene HL Wide complex tachycardia:

misdiagnosis and outcome after emergent therapy Ann Intern Med

1986;104:766–71.

2 Tchou P, Young P, Mahmud R, Denker S, Jazayeri M, Akhtar M Useful

clinical criteria for the diagnosis of ventricular tachycardia Am J Med

1988;84:53–6.

3 Akhtar M, Shenasa M, Jazayeri M, Caceres J, Tchou PJ.Wide QRS complex

tachycardia Reappraisal of a common clinical problem Ann Intern Med

1988;109:905–12.

4 Baerman JM, Morady F, DiCarlo LA, Jr., de Buitleir M Differentiation of ventricular tachycardia from supraventricular tachycardia with

aberration: value of the clinical history Ann Emerg Med 1987;16:40–3

5 Morady F, Baerman JM, DiCarlo LA, Jr., DeBuitleir M, Krol RB, Wahr DW.

A prevalent misconception regarding wide-complex tachycardias JAMA

1985;254:279–2

6 Kindwall KE, Brown J, Josephson ME Electrocardiographic criteria for ventricular tachycardia in wide complex left bundle branch block

morphology tachycardias Am J Cardiol 1988;61:1279–83

7 Brugada P, Brugada J, Mont L, Smeets J, Andries EW A new approach to the differential diagnosis of a regular tachycardia with a wide QRS

complex [see comments] Circulation 1991;83:1649–59.

8 Dancy M, Ward D Diagnosis of ventricular tachycardia: a clinical

algorithm BMJ 1985;291:1036–8.

9 Griffith MJ, Garratt CJ, Mounsey P, Camm AJ Ventricular tachycardia as

default diagnosis in broad complex tachycardia Lancet 1994;343:386–8.

10 Griffith MJ, Linker NJ, Ward DE, Camm AJ Adenosine in the diagnosis

of broad complex tachycardia Lancet 1988;i:672–5.

11 Rankin AC, Oldroyd KG, Chong E, Rae AP, Cobbe SM Value and limitations of adenosine in the diagnosis and treatment of narrow and

broad complex tachycardias Br Heart J 1989;62:195–203.

12 Rankin AC, Rae AP, Cobbe SM Misuse of intravenous verapamil in

patients with ventricular tachycardia Lancet 1987;2:472–4.

13 Garratt CJ, Griffith MJ, Young G, et al Value of physical signs in the

diagnosis of ventricular tachycardia Circulation 1994;90:3103–7.

14 Wellens HJ, Bar FW, Lie KI The value of the electrocardiogram in the Cardiovascular Emergencies

differential diagnosis of a tachycardia with a widened QRS complex Am

J Med 1978;64:27–33.

15 Griffith MJ, de Belder MA, Linker NJ, Ward DE, Camm AJ Multivariate analysis to simplify the differential diagnosis of broad complex

tachycardia Br Heart J 1991;66:166–74.

16 Wellens HJ, Brugada P Diagnosis of ventricular tachycardia from the

12-lead electrocardiogram Cardiol Clin 1987;5:511–25.

17 Rankin AC, Brooks R, Ruskin JN, McGovern BA Adenosine and the

treatment of supraventricular tachycardia Am J Med 1992;92:655–64.

18 van der Watt MJ, Aboo M, Millar RN A prospective study of electrical

cardioversion for sustained tachycardias by emergency unit personnel S

Afr Med J 1995;85:508–11

19 Gorgels AP, van den Dool A, Hofs A, et al Comparison of procainamide

and lidocaine in terminating sustained monomorphic ventricular

tachycardia [see comments] Am J Cardiol 1996;78:43–6.

20 Ho DS, Zecchin RP, Richards DA, Uther JB, Ross DL Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained

ventricular tachycardia [see comments] Lancet 1994;344:18–23

21 Scheinman MM, Levine JH, Cannom DS, et al Dose-ranging study of

intravenous amiodarone in patients with life-threatening ventricular tachyarrhythmias The Intravenous Amiodarone Multicenter

Investigators Group [see comments] Circulation 1995;92:3264–72.

22 Levine JH, Massumi A, Scheinman MM, et al Intravenous amiodarone

for recurrent sustained hypotensive ventricular tachyarrhythmias.

Intravenous Amiodarone Multicenter Trial Group J Am Coll Cardiol

clinical and hypothetical considerations PACE 1983;6:1094.

25 Roden DM The long QT syndrome and torsade de pointes: basic and

clinical aspects In: El-Sherif N, Somel P, eds Cardiac pacing and

electrophysiology Philadelphia: WB Saunders, 1991.

26 Viskin S, Belhassen B Polymorphic ventricular tacharrhythmias in the

absence of organic heart disease Prog Cardiovasc Dis 1998;41:17–34.

12: Syncope,

bradyarrhythmias, and

temporary cardiac pacing

J FERGUSON, KM CHANNON, Y BASHIR

12.1 Introduction

12.2 Syncope

12.2.1 Causes of syncope 12.2.2 Diagnostic approach:

12.3 Bradyarrhythmias

12.3.1 Presentations 12.3.2 Classification:

12.3.3 Assessment and indications for pacing 12.4 Bradyarrhythmias and temporar y pacing in acute myocardial infarction

12.1 Introduction

This chapter deals with the acute management ofbradyarrhythmias and the interrelated clinical problem ofpatients presenting with “syncope, ? cause” In cases ofpersistent bradycardia, for example a patient admitted incomplete heart block, diagnosis is straightforward from a 12-lead ECG or rhythm strip Intermittent bradyarrhythmias pose

a much more difficult challenge The patient presents in sinusrhythm and the diagnosis is suspected because of a history ofone or more preceding episodes of altered consciousness(syncope or presyncope) However, syncope is a commonsymptom in the population, with an incidence of perhaps20–40% in young adults and 25% or more in the elderly (over

75 years) Only a few of these cases are caused by brady- ortachyarrhythmias and the majority are due to vasodepressormechanisms, particularly neurocardiogenic syncope(including vasovagal faints) and related disorders.1 Similarly,syncope accounts for at least 3% of referrals to acute medical

units but only a small minority turn out to have anarrhythmic basis Nevertheless, most of these patients areadmitted, and an increasing number are being subsequentlyreferred for consideration of permanent pacemakers despitelittle supporting evidence, reflecting the undue concern ofmany hospital doctors about the possibility ofbradyarrhythmias Factors that may have contributed to thisovercautious approach include:

• Traditional clinical teaching stresses the associationbetween classical Stokes–Adams attacks andbradyarrhythmias (particularly heart block), with too littleemphasis given to other (commoner) causes of syncope

• Hospital doctors are often not familiar with theepidemiology of syncope in the community

• Many clinicians are unaware that neurocardiogenicsyncope can produce abrupt loss of consciousness withoutclassical autonomic prodromal symptoms or triggeringcircumstances in some cases, especially among the elderly

In dealing with patients who have been referred because ofsyncope, the priority in the acute setting is to identify thosecases (the majority) who can be discharged directly andinvestigated on an outpatient basis However, admission isrequired2 if: the patient is considered at risk of sudden death(those with structural heart disease or other clues toventricular tachyarrhythmias); there is evidence ofbradycardia (particularly atrioventricular (AV) block) likely torequire temporary or permanent cardiac pacing; the syncopalattacks are occurring frequently (daily or more often); or thepatient is elderly and/or considered at risk of serious injury

12.2 Syncope

Syncope is defined as sudden, transient loss of consciousnessdue to reduced cerebral blood flow It is a very commonsymptom, exhibiting a biomodal distribution with peaksamong adolescents/young adults and the elderly.3 Recentresearch has shown that many unexplained falls or dropattacks in the elderly are also attributable to syncope withamnesia for the event itself, so that the patient denies any loss

of consciousness.4The historic term “Stokes–Adams” attack islargely redundant in modern clinical practice and shouldprobably be avoided It referred to the features observedduring a profound, transient bradyarrhythmia, typicallyabrupt loss of consciousness and associated pallor, followed byprompt recovery with minimal autonomic features.

be identified in around 35% of cases, recent data suggests thatmost of these would also have been due to neurocardiogenicmechanisms

Box 12.1 Causes of syncope

Neurocardiogenic or neurally mediated syncope

Polymorphic VT (including long QT syndromes)

Supraventricular tachycardia (uncommon)

Box 12.2 Pathophysiology of neurocardiogenic syncopeThe pathophysiology of neurocardiogenic syncope is not completely understood but the basic mechanisms of vasovagal syncope, carotid sinus syndrome and situational (cough, micturition, and swallow) syncope all have three common components: (i) the afferent limb; (ii) central ner vous system; and (iii) the efferent limb (Figure 12.1) The afferent signals emanate mainly from peripheral mechanical, chemical, pain, or temperature receptors but also from the central ner vous system itself (the sight of blood, fear, anxiety, etc.) These stimuli transmit impulses predominantly to the nucleus solitarius in the medulla, a site closely related to the dorsal and ambiguus nuclei

of the vagus ner ve In vasovagal syncope, venous pooling to the lower extremities reduces venous return to the hear t Reflex sympathetic stimulation and sinus tachycardia commonly precede the neurocardiogenic reaction The combination of a sudden reduction in ventricular volume and forceful ventricular contraction trigger cardiopulmonar y mechanoreceptors which would normally only be activated by the mechanical stretch of volume or pressure loading After CNS processing, the efferent limb of the reflex is mediated by increased parasympathetic outflow and reduced sympathetic activity causing the bradycardia and vasodilatation that are characteristic of neurocardiogenic syncope The bradycardia, which may be profound

in some patients but only relative in others, is vagally mediated Vasodilatation, on the other hand, depends on the interaction in sympathetic and parasympathetic tone Release of acetylcholine from the parasympathetic system inhibits noradrenaline release from sympathetic ner ve endings Similarly, release of noradrenaline and neuropeptide Y from sympathetic ner ve endings inhibits the release

of acetylcholine from the parasympathetic system As a result, the temporal sequence as well as the magnitude of sympathetic or parasympathetic responses are impor tant in the evolution of neurocardiogenic syncope.

Although the central mechanisms contributing to this response are not clear, the role of endogenous opiates and serotonin have been studied closely and both are probably involved in the inappropriate vasodepressor response to acute haemorrhage Studies using serotonin reuptake inhibitors, such as fluoxetine, ser traline, and paroxetine, have shown promising results in the treatment of neurocardiogenic syncope The role of the carotid and aor tic baroreceptors in neurocardiogenic syncope is likely to be impor tant Under normal circumstances these receptors would respond to hypotension by increasing sympathetic tone However, for reasons that are unclear, this feedback mechanism seems to be blunted in neurocardiogenic syncope.

Neurocardiogenic syncope encompasses all forms of syncopedue to neurally-mediated reflex vasomotor instability (Box12.2, Figure 12.1) The group includes the common vasovagalfaint, situational syncope (triggered by cough, micturition,etc.), carotid sinus syncope, and exertional syncope associatedwith aortic stenosis or pulmonary hypertension Confusionmay arise from some of the terminology used.

“Neurocardiogenic syncope”, strictly speaking, applies to theentire group but is often used loosely to refer to the commonvasovagal faint The term “malignant vasovagal syndrome” isused to describe any cases of neurocardiogenic syncope inwhich there is abrupt loss of consciousness without prodromalautonomic symptoms, and hence a risk of serious injury.These conditions all involve a complex interplay of neural andcardiovascular reflexes5 organised into: (i) an afferent limb(e.g cardiopulmonary mechanoreceptors in vasovagalsyncope); (ii) central nervous system (CNS) connections andprocessing (predominantly within the medulla); and (iii) anefferent limb acting via the twin mechanisms of vagally-mediated bradycardia (the “cardio-inhibitory response”) andvasodilatation due to withdrawal of sympathetic tone (the

“vasodepressor response”) It is not generally appreciated that

EFFERENT PATHWAYS Vasovagal Faint

(pain, stress, anxiety)

Carotid Baroreceptors

Cardiac Chemoreceptors

Mechanoreceptors Airway/Pulmonary Receptors

GI/GU Mechanoreceptors

Feedback via Carotid Barorecptors

Bradycardia/ Hypotension

the vasodepressor component is usually the dominantmechanism leading to cerebral hypoperfusion6 and loss ofconsciousness, often with normal heart rates or only relativebradycardia (40–60 bpm) Even in patients exhibiting severebradycardia, there may be a major co-existent vasodepressorcomponent, with the result that even AV sequential pacingmay not prevent syncope.

The two main groups of bradyarrhythmias are sino-atrialdisease (also known as sinus node disease, sick sinus syndrome,brady-tachy syndrome, etc.) which is usually a result of chronicidiopathic conduction system fibrosis, or atrioventricularconduction disease which may result from fibrosis, ischaemicheart disease, or cardiomyopathies.7 Sino-atrial and AVconduction quite often co-exist in the same patient

Ventricular tachyarrhythmias (VT) represent a relativelyuncommon but particularly important cause of syncope,because these patients are at high risk of sudden death.Sustained monomorphic VT usually arises in the context ofischaemic heart disease and prior myocardial infarction.Polymorphic ventricular tachycardia may be a manifestation

of myocardial ischaemia during an acute coronary syndrome

or may arise from congenital or acquired forms of long QTsyndrome (see Chapter 11) Syncope is also surprisinglycommon among patients with paroxysmal supraventriculartachycardia,5 but may be primarily due to a co-existentneurocardiogenic reaction in most cases; however, theprognosis is benign

Postural hypotension is most usually due to autonomicdysfunction or age-related physiological changes but is oftenexacerbated by volume depletion or medication

An important point that emerges from all published series isthat syncope occurring in the setting of structural heartdisease (most commonly ischaemic heart disease) is associatedwith a poor prognosis,2 compared to syncope occurring inpatients with no heart disease, regardless of the mechanism.This reflects the association of life threatening arrhythmiaswith cardiac disease